This document provides guidelines on the diagnosis and management of syncope. It defines syncope and provides a brief overview of the pathophysiology. The document is divided into four parts: classification, epidemiology and prognosis; diagnosis; treatment; and special issues in evaluating patients with syncope. The guidelines aim to provide recommendations on diagnostic criteria, diagnostic workup, risk stratification, and determining when hospitalization is needed. Most recommendations are based on consensus expert opinion due to the lack of randomized controlled trials in this area.
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Sincope guidelines
1. European Heart Journal (2001) 22, 1256–1306
doi:10.1053/euhj.2001.2739, available online at http://www.idealibrary.com on
Task Force Report
Guidelines on management (diagnosis and treatment)
of syncope*
Task Force on Syncope, European Society of Cardiology†: M. Brignole (Chairman),
P. Alboni, D. Benditt, L. Bergfeldt, J. J. Blanc, P. E. Bloch Thomsen, J. G. van Dijk,
A. Fitzpatrick, S. Hohnloser, J. Janousek, W. Kapoor, R. A. Kenny, P. Kulakowski,
A. Moya, A. Raviele, R. Sutton, G. Theodorakis and W. Wieling
Table of contents
Preamble
Scope of the document 1256
Method 1257
Part 1. Classification, epidemiology and prognosis
Definition 1258
Brief overview of pathophysiology of syncope 1258
Classification 1259
Epidemiological considerations 1259
Prognostic stratification: identification of factors
predictive of adverse outcome 1260
Part 2. Diagnosis
Strategy of evaluation (flow chart) 1262
Initial evaluation (history, physical examination,
baseline electrocardiogram) 1264
Echocardiogram 1266
Carotid sinus massage 1266
Tilt testing 1268
Electrocardiographic monitoring (non-invasive
and invasive) 1271
Electrophysiological testing 1273
ATP test 1277
Ventricular signal-averaged electrocardiogram 1278
Exercise testing 1278
Cardiac catheterization and angiography 1279
Neurological and psychiatric evaluation 1279
Diagnostic yield and prevalence of causes
of syncope 1282
Part 3. Treatment
General principles 1282
Neurally-mediated reflex syncopal syndromes 1283
Orthostatic hypotension 1285
Cardiac arrhythmias as primary cause 1286
Structural cardiac or cardiopulmonary disease 1289
Vascular steal syndromes 1289
Metabolic 1290
Part 4. Special issues in evaluating patients with syncope
Need for hospitalization 1290
Syncope in the older adult 1290
Syncope in paediatric patients 1292
Driving and syncope 1293
Glossary of uncertain terms 1293
Preamble
Scope of the document
The purpose of this document is to provide specific
recommendations on the diagnostic evaluation and
management of syncope. The document is divided into
four parts: (1) classification, epidemiology and prog-
nosis; (2) diagnosis; (3) treatment; and (4) special issues
in evaluating patients with syncope. Each part reviews
background information and summarizes the relevant
literature. The details of pathophysiology and mech-
anisms of various aetiologies were considered to lie
outside the scope of this document. Although the docu-
ment encompasses many of the important aspects of
syncope, the panel recommendations focused on the
following main questions:
1. What are the diagnostic criteria for causes of
syncope?
2. What is the preferred approach to the diag-
nostic work-up in various subgroups of patients with
syncope?
3. How should patients with syncope be risk stratified?
Correspondence: Michele Brignole, MD, FESC, Department of
Cardiology and Arrhythmologic Centre, Ospedali Riuniti, 16033
Lavagna, Italy.
*This document has been reviewed by members of the Committee
for Practice Guidelines (formerly Committee for Scientific and
Clinical Initiatives) and by the members of the Board of the
European Society of Cardiology (see Appendix 1), who approved
the document on 8 March 2001. The full text of this document is
available on the website of the European Society of Cardiology in
the section ‘Scientific Information’, Guidelines.
†For affiliations of Task Force members see Appendix 2.
0195-668X/01/221256+51 $35.00/0 2001 The European Society of Cardiology
2. 4. When should patients with syncope be hospitalized?
5. Which treatments are likely to be effective in prevent-
ing syncopal recurrences?
Method
The methodology for writing this document consisted of
literature reviews and consensus development by the
panel assembled by the European Society of Cardiology.
The panel met in August 1999 and developed a compre-
hensive outline of the issues that needed to be addressed
in the document. Subgroups of the panel were formed
and each was assigned the task of reviewing the litera-
ture on a specific topic and of developing a draft
summarizing the issue. Each subgroup was to perform
literature searches on MEDLINE and to supplement the
search by documents from their personal collection. The
panel reconvened in January 2000, reviewed the draft
documents, made revisions whenever appropriate and
developed the consensus recommendations. The panel
discussed each recommendation and arrived at consen-
sus by obtaining a majority vote. When there was
divergence of opinion, this was noted. Since the goal of
the project was to provide specific recommendations for
diagnosis and management, guidelines are provided even
when the data from the literature is not definitive. It
must be pointed out that most of the recommendations
are based on consensus expert opinion. All the members
of the panel reviewed final drafts of the document and
their comments were incorporated. If changes in recom-
mendations were suggested, these were brought to vote
in a second meeting in August 2000. The executive
committee met in February 2001 to consider the com-
ments of external reviewers, and to make amendments.
Finally, the document was discussed with the Presidents
of the National Societies in March 2001.
A major issue in the use of diagnostic tests is that
syncope is a transient symptom and not a disease.
Typically patients are asymptomatic at the time of
evaluation and the opportunity to capture a spon-
taneous event during diagnostic testing is rare. As a
result, the diagnostic evaluation has focused on physio-
logical states that could cause loss of consciousness. This
type of reasoning leads, of necessity, to uncertainty in
establishing a cause. In other words, the causal relation-
ship between a diagnostic abnormality and syncope in a
given patient is often presumptive. Uncertainty is further
compounded by the fact that there is a great deal of
variation in how physicians take a history and perform a
physical examination, the types of tests requested and
how they are interpreted. These issues make the diag-
nostic evaluation of syncope inordinately difficult. Con-
sequently there is a need for specific criteria to aid
diagnosis from history and physical examination, and
clear-cut guidelines on how to choose tests, how to
evaluate test abnormalities and how to use the results
to establish a cause of syncope. This document has tried
to provide specific criteria by using the literature as well
as a consensus of the panel.
A further concern about tests for evaluating the aeti-
ology of syncope is that it is not possible to measure test
sensitivity because there is no reference or gold standard
for most of the tests employed for this condition. Since
syncope is an episodic symptom, a reference standard
could be an abnormality observed during a spontaneous
event. However, this is only rarely possible, for instance,
if an arrhythmia occurred concurrently with syncope.
These instances are uncommon, however, and most of
the time decisions have to be made based on a patient’s
history or abnormal findings during asymptomatic
periods. To overcome the lack of a gold standard, the
diagnostic yield of many tests in syncope has been
assessed indirectly by evaluating the reduction of syncopal
recurrences after administration of the specific therapy
suggested by the results of the test which were diagnostic.
The literature on syncope testing is largely composed
of case series, cohort studies, or retrospective analyses of
already existing data. The impact of testing on guiding
therapy and reducing syncopal recurrences is difficult
to discern from these methods of research without
randomization and blinding. Because of these issues, the
panel performed full reviews of the literature for diag-
nostic tests but did not use pre-defined criteria for
selection of articles to be reviewed. Additionally, the
panel did not feel that an evidence-based summary of
the literature was possible.
In assessing treatment of syncope, this document
reviews the few randomized-controlled trials that have
been reported. For various diseases and disorders with
known treatments (e.g. orthostatic hypotension, sick
sinus syndrome) those therapies are reviewed and rec-
ommendations are modified for patients with syncope.
Most studies of treatment have used a non-randomized
design and many even lack a control group. The
interpretation of these studies is very difficult but
their results were used in summary recommendations of
treatment.
The strength of recommendations has been ranked as
follows:
3. Class I, when there is evidence for and/or general
agreement that the procedure or treatment is useful.
Class I recommendations are generally those reported
in the sections headed ‘Recommendations’ and in the
Tables.
4. Class II, when usefulness of the procedure or treat-
ment is less well established or divergence of opinion
exists among the members of the Task Force.
5. Class III, when the procedure or treatment is not
useful and in some cases may be harmful.
The strength of evidence supporting a particular
procedure/treatment option has been ranked as follows:
6. Level of Evidence A=Data derived from multiple
randomized clinical trials or meta-analyses.
7. Level of Evidence B=Data derived from a single
randomized trial or multiple non-randomized studies.
8. Level of Evidence C=Consensus Opinion of experts.
When not expressed otherwise, evidence is of type C.
Task Force Report 1257
Eur Heart J, Vol. 22, issue 15, August 2001
9. Part 1. Classification, epidemiology
and prognosis
Definition
Syncope (derived from the Greek words, ‘syn’ meaning
‘with’ and the verb ‘koptein’ meaning ‘to cut’ or more
appropriately in this case ‘to interrupt’) is a symptom,
defined as a transient, self-limited loss of consciousness,
usually leading to falling. The onset of syncope is
relatively rapid, and the subsequent recovery is
spontaneous, complete, and usually prompt[1–3]
. The
underlying mechanism is a transient global cerebral
hypoperfusion.
In some forms of syncope there may be a premonitory
period in which various symptoms (e.g. light-
headedness, nausea, sweating, weakness, and visual
disturbances) offer warning of an impending syncopal
event. Often, however, loss of consciousness occurs
without warning. Recovery from syncope is usually
accompanied by almost immediate restoration of appro-
priate behaviour and orientation. Retrograde amnesia,
although believed to be uncommon, may be more fre-
quent than previously thought, particularly in older
individuals. Sometimes the post-recovery period may be
marked by fatigue.
An accurate estimate of the duration of syncope
episodes is rarely obtained. However, typical syncopal
episodes are brief. Complete loss of consciousness in
vasovagal syncope is usually no longer than 20 s in
duration. In one videometric study of 56 episodes of
short-lasting severe cerebral hypoxia in adolescents
induced by an instantaneous deep fall in systemic
pressure using the ‘mess trick’, syncope occurred in all
without any premonitory symptoms, and myoclonic
jerks were present in 90%; the syncope duration
averaged 12 s (range 5–22)[2]
. However, rarely syncope
duration may be longer, even lasting for several minutes.
In such cases, the differential diagnosis between syncope
and other causes of loss of consciousness can be
difficult[3]
.
Pre-syncope or near-syncope refers to a condition in
which patients feel as though syncope is imminent.
Symptoms associated with pre-syncope may be relatively
non-specific (e.g. ‘dizziness’), and tend to overlap with
those associated with the premonitory phase of true
syncope described earlier.
Brief overview of pathophysiology of
syncope
Specific factors resulting in syncope vary from patient to
patient, but several general principles are worthy of
note.
In healthy younger individuals with cerebral blood
flow in the range of 50–60 ml/100 g tissue/min — that
represents about 12 to 15% of resting cardiac
output — minimum oxygen requirements necessary to
sustain consciousness (approximately 3·0 to 3·5 ml O2/
100 g tissue/min) are easily achieved[4]
. However, in
older individuals, or those with underlying disease con-
ditions, the safety factor for oxygen delivery may be
more tenuous[5–7]
.
Cerebral perfusion pressure is largely dependent on
systemic arterial pressure. Thus, any factor that
decreases either cardiac output or total peripheral
vascular resistance diminishes systemic arterial pressure
and cerebral perfusion pressure[8]
. In regard to cardiac
output, the most important physiological determinant is
venous filling. Therefore, excessive pooling of blood in
dependent parts of the body or diminished blood volume
may predispose to syncope. Cardiac output may also be
impaired due to bradyarrhythmias, tachyarrhythmias,
or valvular disease. In terms of peripheral vascular
resistance, widespread and excessive vasodilatation may
play a critical role in decreasing arterial pressure (a main
cause of fainting in the reflex syncopal syndromes).
Vasodilatation also occurs during thermal stress.
Impaired capacity to increase vascular resistance during
standing is the cause of orthostatic hypotension and
syncope in patients using vasoactive drugs and in
patients with autonomic neuropathies[9]
. Cerebral
hypoperfusion may also result from an abnormally high
cerebral vascular resistance. Low carbon dioxide tension
is probably the main cause, but sometimes the cause
remains unknown.
A sudden cessation of cerebral blood flow for 6 to 8 s
has been shown to be sufficient to cause complete loss of
consciousness[1]
. Experience from tilt testing showed
that a decrease in systolic blood pressure to 60 mmHg is
associated with syncope[10]
. Further, it has been esti-
mated that as little as a 20% drop in cerebral oxygen
delivery is sufficient to cause loss of consciousness[1]
. In
this regard, the integrity of a number of control mech-
anisms is crucial for maintaining adequate cerebral
nutrient delivery, including: (a) cerebrovascular ‘auto-
regulatory’ capability, which permits cerebral blood
flow to be maintained over a relatively wide range of
perfusion pressures; (b) local metabolic and chemical
control which permits cerebral vasodilatation to occur in
the presence of either diminished pO2 or elevated pCO2;
(c) arterial baroreceptor-induced adjustments of heart
rate, cardiac contractility, and systemic vascular resist-
ance, which modify systemic circulatory dynamics in
order to protect cerebral flow; (d) and vascular volume
regulation, in which renal and hormonal influences help
to maintain central circulating volume.
Transient failure of protective mechanisms, or the
intervention of other factors (e.g. drugs, haemorrhage)
which reduce systemic pressure below the autoregula-
tory range for an extended period of time, may induce a
syncopal episode. Risk of failure is greatest in older or ill
patients[5,6,11]
. Ageing alone has been associated with
diminution of cerebral blood flow[5,6]
. Additionally,
certain common disease states may diminish cerebral
blood flow protection. For example, hypertension has
been associated with a shift of the autoregulatory range
to higher pressures, while diabetes alters the chemo-
receptor responsiveness of the cerebrovascular bed[7]
.
1258 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
10. Classification
Syncope must be differentiated from other ‘non-
syncopal’ conditions associated with real or apparent
transient loss of consciousness (Fig. 1). Table 1.1 and 1.2
provide a pathophysiological classification of the princi-
pal known causes of transient loss of consciousness. The
subdivision of syncope is based on pathophysiology as
follows:
11. ‘Neurally-mediated reflex syncopal syndrome’ refers
to a reflex that, when triggered, gives rise to vaso-
dilatation and bradycardia, although the contribu-
tion of both to systemic hypotension and cerebral
hypoperfusion may differ considerably.
12. ‘Orthostatic’ syncope occurs when the autonomic
nervous system is incapacitated resulting in a failure
of vasoconstrictor mechanisms and thereby in ortho-
static hypotension; ‘Volume depletion’ is another
important cause of orthostatic hypotension and
syncope.
13. ‘Cardiac arrhythmias’ can cause a decrease in
cardiac output, which usually occurs irrespective of
circulatory demands.
14. ‘Structural heart disease’ can cause syncope when
circulatory demands outweigh the impaired ability of
the heart to increase its output.
15. ‘Steal’ syndromes can cause syncope when a blood
vessel has to supply both part of the brain and an
arm.
Several disorders resemble syncope in two different
ways. In some, consciousness is impaired or lost as a
result of metabolic disorders (including hypoxia, hyper-
ventilation with hypocapnia, hypoglycaemia), epilepsy
and intoxication. In several other disorders, conscious-
ness is only apparently lost; this is the case with soma-
tization disorders, cataplexy and drop attacks. Table 1.2
lists the most common conditions misdiagnosed as the
cause of syncope. It should be noted that the conditions
listed here do not result from sudden transient global
cerebral hypoperfusion. A differentiation such as this is
important because the clinician is usually confronted
with patients whose sudden loss of consciousness may be
due to causes not associated with decreased cerebral
blood flow such as seizure and/or conversion reaction.
A major limitation of this classification is the fact that
more than one pathophysiological factor may contribute
to the symptoms. For instance, in the setting of valvular
aortic stenosis or left ventricular outflow tract obstruc-
tion, syncope is not solely the result of restricted cardiac
output, but may, in part, be due to inappropriate
neurally mediated reflex vasodilation and/or primary
cardiac arrhythmias[12]
. Similarly, a neural reflex com-
ponent (preventing or delaying vasoconstrictor compen-
sation) appears to play an important role when syncope
occurs in association with certain brady- and
tachyarrhythmias[13–15]
.
Epidemiological considerations
Numerous studies have examined epidemiological
aspects of syncope and delineated the multiple potential
causes of syncope. However, some reports have focused
on relatively select populations such as the military,
or tertiary care medical centres or solitary medical
practices. For example, a survey of 3000 United States
Air Force personnel (average age 29 years) revealed that
27% had experienced a syncopal spell during their
lifetime[16]
. Application of these findings to medical
practice is limited not only by the nature of the environ-
ment in which patients were enrolled, but also the
variable manner in which symptoms were evaluated.
In terms of studies examining a broad population
sample, the Framingham Study (in which biennial
• Neurally-mediated reflex syncopal
syndromes
Cardiac arrhythmias as primary
cause
•
• Structural cardiac or
cardiopulmonary disease
Real or apparent transient loss of consciousness
Non-syncopal:Syncope:
Orthostatic•
Cerebrovascular•
• Disorders resembling syncope
with impairment or loss of
consciousness, e.g. seizure
disorders, etc
• Disorders resembling syncope
without loss of consciousness,
e.g. psychogenic syncope
(somatization disorders), etc
Figure 1 Classification of transient loss of consciousness.
Task Force Report 1259
Eur Heart J, Vol. 22, issue 15, August 2001
16. examinations were carried out over a 26-year period in
5209 free-living individuals, 2336 men and 2873 women)
reported at least one syncopal event during the study
period in approximately 3% of men and 3·5% of
women[17]
. The mean initial age of first syncope was
52 years (range 17 to 78 years) for men, and 50 years
(range 13 to 87 years) for women. Further, prevalence of
isolated syncope (defined as syncope in the absence of
prior or concurrent neurological, coronary, or other
cardiovascular disease stigmata) increased from 8 per
1000 person-exams in the 35–44-year-old age group,
to approximately 40 per 1000 person-exams in the
d75-year-old age group. These data, however, are in
conflict with studies reported from selected populations
such as among the elderly confined to long-term care
institutions, where the annual incidence may be as high
as 6% with a recurrence rate of 30%[18]
. Several reports
indicate that syncope is a common presenting problem
in health care settings, accounting for 3% to 5% of
emergency room visits and 1% to 3% of hospital
admissions[19–21]
.
Other studies in specific populations provide insight
into the relative frequency with which syncope may
occur in certain settings. Several of these reports may be
summarized as follows:
20. 16% during a 10-year period in men aged 40–59[25]
21. 19% during a 10-year period in women aged 40–49[25]
22. 23% during a 10-year period in elderly people (age
70)[18]
However, the majority of these individuals probably do
not seek medical evaluation.
In summary, even if some variability in prevalence
and incidence of syncope is reported, the majority of
studies suggest that syncope is a common problem in the
community, long-term care institutions, and in health
care delivery settings.
Prognostic stratification: identification of
factors predictive of adverse outcome
Mortality
Studies in the 1980s showed that 1-year mortality of
patients with cardiac syncope was consistently higher
Table 1.1 Causes of syncope
Neurally-mediated reflex syncopal syndromes
40. Vascular steal syndromes
Table 1.2 Causes of non-syncopal attacks (commonly misdiagnosed as syncope)
Disorders with impairment or loss of consciousness
48. Transient ischaemic attacks (TIA) of carotid origin
#Disturbance of consciousness probably secondary to metabolic effects on cerebrovascular tone.
*May also include hysteria, conversion reaction.
1260 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
49. (ranging between 18–33%) than patients with non-
cardiac cause (0–12%) or unexplained syncope
(6%)[19,20,26–28]
. One-year incidence of sudden death was
24% in patients with a cardiac cause compared with
3–4% in the other two groups[27,28]
. When adjustments
were made for differences in baseline rates of heart and
other diseases, cardiac syncope was still an independent
predictor of mortality and sudden death[27,28]
. However,
a more recent study directly compared the outcomes of
patients with syncope with matched control subjects
without syncope[29]
. Although patients with cardiac syn-
cope had higher mortality rates compared with those of
non-cardiac or unknown causes, patients with cardiac
causes did not have a higher mortality when compared
with their matched controls with similar degrees of heart
disease[29]
. This study showed that the presence of struc-
tural heart disease was the most important predictor of
mortality. In a selected population of patients with
advanced heart failure and a mean ejection fraction of
20%, the patients with syncope had a higher risk of
sudden death (45% at 1 year) than those without (12%
at 1 year); admittedly, the risk of sudden death was
similarly high in patients with either supposed cardiac
syncope or syncope from other causes[30]
.
Structural heart disease is a major risk factor for
sudden death and overall mortality in patients with
syncope. The association of syncope with aortic stenosis
has long been recognized as having an average survival
without valve replacement of 2 years[31]
. Similarly, in
hypertrophic cardiomyopathy, the combination of
young age, syncope at diagnosis, severe dyspnoea and a
family history of sudden death best predicted sudden
death[32]
. In arrhythmogenic right ventricular dysplasia,
patients with syncope or symptomatic ventricular tachy-
cardia have a similarly poor prognosis[33]
. Patients with
ventricular tachyarrhythmias have higher rates of mor-
tality and sudden death but the excess mortality rates
depend on underlying heart disease; patients with severe
ventricular dysfunction have the worst prognosis[34]
.
Some of the cardiac causes of syncope do not appear to
be associated with increased mortality. These include
most types of supraventricular tachycardias and sick
sinus syndrome.
A number of subgroups of patients can be identified
which have an excellent prognosis. Certain of these
include:
50. Young healthy individuals without heart disease and
normal ECG. The 1-year mortality and sudden death
rates in young patients (less than 45 years of age)
without heart disease and normal ECG is low[35]
.
Although comparisons have not been made with age-
and sex-matched controls, there is no evidence that
these patients have an increased mortality risk. Many
of these patients have neurally mediated syncope or
unexplained syncope.
51. Neurally mediated syndromes. A large number of
cohort studies in which the diagnosis has been estab-
lished using tilt testing show that the mortality at
follow-up of patients with neurally mediated syncope
is near 0%[36]
. Most of these patients had normal
hearts. None of these studies report patients who died
suddenly.
52. Orthostatic hypotension. The mortality rates of
patients with orthostatic hypotension depend on the
causes of this disorder. Many of the causes (e.g.
volume depletion, drug-induced) are transient prob-
lems that respond to treatment and do not have
long-term consequences. Disorders of the autonomic
system have health consequences and may potentially
increase mortality depending on the severity of the
disease. In the elderly patients with orthostatic
hypotension, the prognosis is largely determined by
co-morbid illnesses.
53. Syncope of unknown cause. An approximately 5% first
year mortality in patients with unexplained syncope
has been a relatively consistent observation in the
literature[19,20,27,28,37]
. Although the mortality is
largely due to underlying co-morbidity, such patients
continue to be at risk for physical injury, and may
encounter employment and life-style restrictions.
Recurrences
Approximately 35% of patients have recurrences of
syncope at 3 years of follow-up; 82% of recurrences
occur within the first 2 years[28,38]
. Predictors of recur-
rence of syncope include having had recurrent syncope
at the time of presentation (four or more episodes in
one study[38]
) or a psychiatric diagnosis[38–40]
. In one
study[41]
, more than five lifetime episodes gave a 50%
chance of recurrence in the following year. In another
study[39]
, age 45 years was also associated with higher
rates of syncopal recurrence after controlling for other
risk factors. After positive tilt table testing the
patients with more than six syncopal spells had a risk
of recurrence of 50% over 2 years[42]
.
Recurrences are not associated with increased mor-
tality or sudden death rates, but patients with recurrent
syncope have a poor functional status similar to patients
with other chronic diseases.
Risk stratification
One study has developed and validated a clinical predic-
tion rule for risk stratification of patients with syn-
cope[35]
. This study used a composite outcome of having
cardiac arrhythmias as a cause of syncope or death (or
cardiac death) within 1 year of follow-up. Four variables
were identified and included age d45 years, history of
congestive heart failure, history of ventricular arrhyth-
mias, and abnormal ECG (other than non-specific ST
changes). Arrhythmias or death within 1 year occurred
in 4–7% of patients without any of the risk factors and
progressively increased to 58–80% in patients with three
or more factors[35]
. The critical importance of identifying
cardiac causes of syncope is that many of the arrhyth-
mias and other cardiac diseases are now treatable with
drugs and/or devices.
Physical injury
Syncope may result in injury to the patient or to others
such as may occur when a patient is driving. Major
Task Force Report 1261
Eur Heart J, Vol. 22, issue 15, August 2001
54. morbidity such as fractures and motor vehicle accidents
were reported in 6% of patients and minor injury such as
laceration and bruises in 29%. There is no data on the
risk of injury to others. Recurrent syncope is associ-
ated with fractures and soft-tissue injury in 12% of
patients[38]
.
Quality of life
A study that evaluated the impact of recurrent syncope
on quality of life in 62 patients used the Sickness Impact
Profile and found functional impairment similar to
chronic illnesses such as rheumatoid arthritis, low back
pain, and psychiatric disorders[43]
. Another study on 136
patients with unexplained syncope found impairment on
all five dimensions measured by the EQ-5D instrument,
namely Mobility, Usual activities, Self-care, Pain/
Discomfort, Anxiety/depression. Furthermore there was
a significant negative relationship between frequency of
spells and overall perception of health[41]
.
Economic implications
Patients with syncope are often admitted to hospital and
undergo expensive and repeated investigations, many of
which do not provide a definite diagnosis. A study in
1982 showed that patients often underwent multiple
diagnostic tests despite which a cause of syncope was
established in only 13 of 121 patients[44]
. With the advent
of newer diagnostic tests (e.g. tilt testing, wider use of
electrophysiological testing, loop monitoring) it is likely
that patients are undergoing a greater number of tests at
considerably higher cost. In a recent study, based on
administrative data from Medicare, there were estimated
to be 19 3164 syncope hospital discharges in 1993 in the
U.S.A.[45]
. The cost per discharge was calculated as
$4132 and increased to $5281 for those patients who
were readmitted for recurrent syncope. This figure
underestimates the true total cost associated with
syncope because many patients with syncope are not
admitted to hospital for either investigation or therapy.
Part 2. Diagnosis
Strategy of evaluation
Figure 2 shows a flow diagram of an approach to the
evaluation of syncope.
Initial evaluation
The starting point for the evaluation of syncope is a
careful history and physical examination including
orthostatic blood pressure measurements. In most
young patients without heart disease a definite diagnosis
of neurally mediated syncope can be made without any
further examination. Other than this, a 12-lead ECG
should usually be part of the general evaluation of
patients. This basic assessment will be defined as ‘Initial
evaluation’.
Three key questions should be addressed during the
initial evaluation:
Syncope
History, physical examination, supine and upright BP, standard ECG Initial evaluation
Certain or suspected
diagnosis
Unexplained syncope
Structural heart disease
or abnormal ECG
No structural heart disease
and normal ECG
–+
+ –
Frequent
or severe
Single/rare
Cardiac evaluation
Diagnosis made
Evaluate/confirm
disease/disorder
Re-appraisal
NMS
evaluation
No further
evaluation
TreatmentTreatment Treatment
No
Figure 2 The figure shows the flow diagram proposed by the Task Force on Syncope of an approach to the
evaluation of syncope. BP=blood pressure; ECG=electrocardiogram; NMS=neurally mediated syncope.
1262 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
55.
56. Is loss of consciousness attributable to syncope or
not?
58. Are there important clinical features in the history
that suggest the diagnosis?
Differentiating true syncope from other ‘non-syncopal’
conditions associated with real or apparent transient
loss of consciousness is generally the first diagnostic
challenge and influences the subsequent diagnostic
strategy (see classification in Part 1 and Table 1). Apart
from the prognostic importance of the presence of heart
disease (see Part 1, Prognostic stratification), its absence
excludes a cardiac cause of syncope with few exceptions.
In a recent study[46]
, heart disease was an independent
predictor of a cardiac cause of syncope, with a sensitivity
of 95% and a specificity of 45%; by contrast, the absence
of heart disease ruled out a cardiac cause of syncope in
97% of the patients. Finally, accurate history-taking
may be diagnostic per se of the cause of syncope or may
suggest the strategy of evaluation (see Part 2, Initial
evaluation). It must be pointed out that syncope may be
an accompanying symptom at the presentation of
certain diseases, such as aortic dissection, pulmonary
embolism, acute myocardial infarction, outflow tract
obstruction, etc. In these cases, priority must be given to
specific and immediate treatment of the underlying
condition. These issues are not addressed in this report.
The initial evaluation may lead to a certain or
suspected diagnosis or no diagnosis (here termed as
unexplained syncope).
Certain or suspected diagnosis
Initial evaluation may lead to a certain diagnosis based
on symptoms, signs or ECG findings. The recommended
diagnostic criteria are listed in the section entitled Initial
evaluation. Under such circumstances, no further evalu-
ation of the disease or disorder may be needed and
treatment, if any, can be planned. More commonly, the
initial evaluation leads to a suspected diagnosis, which
needs to be confirmed by directed testing (see Initial
evaluation). If a diagnosis is confirmed by specific test-
ing, treatment may be initiated. On the other hand, if the
diagnosis is not confirmed, then patients are considered
to have unexplained syncope and are evaluated as
follows.
Unexplained syncope
The most important issue in these patients is the pres-
ence of structural heart disease or an abnormal ECG.
These findings are associated with a higher risk of
arrhythmias and a higher mortality at 1 year. In these
patients, cardiac evaluation consisting of echocardiogra-
phy, stress testing and tests for arrhythmia detection
such as prolonged electrocardiographic and loop moni-
toring or electrophysiological study are recommended.
If cardiac evaluation does not show evidence of arrhyth-
mia as a cause of syncope, evaluation for neurally
mediated syndromes is recommended in those with
recurrent or severe syncope.
In patients without structural heart disease and a
normal ECG, evaluation for neurally mediated syncope
is recommended for those with recurrent or severe
syncope. The tests for neurally mediated syncope consist
of tilt testing and carotid massage. The majority of
patients with single or rare episodes in this category
probably have neurally mediated syncope. Since treat-
ment is generally not recommended in this group of
patients, close follow-up without evaluation is recom-
mended. Additional consideration in patients without
structural heart disease and a normal ECG is brady-
arrhythmia or psychiatric illness. Loop monitoring is
needed in patients with recurrent unexplained syncope
whose symptoms are suggestive of arrhythmic syncope.
ATP testing may be indicated at the end of the diag-
nostic work-up. Psychiatric assessment is recommended
in patients with frequent recurrent syncope who have
multiple other somatic complaints and whose initial
evaluation raises concern in terms of stress, anxiety and
other possible psychiatric disorders.
Reappraisal
Once the evaluation, as outlined, is completed and no
cause of syncope is determined, reappraisal of the
work-up is needed since subtle findings or new historical
information may change the entire differential diagnosis.
Reappraisal may consist of obtaining details of history
and reexamining patients as well as a review of the entire
work-up. If unexplored clues to possible cardiac or
neurological disease are apparent, further cardiac and
neurological assessment is recommended. In these cir-
cumstances, consultation with appropriate specialty
services may be needed.
Recommendations
Indications
Class I:
59. Basic laboratory tests are only indicated if syncope
may be due to loss of circulating volume, or if a
syncope-like disorder with a metabolic cause is
suspected.
60. In patients with suspected heart disease, echo-
cardiography, prolonged electrocardiographic monitor-
ing and, if non-diagnostic, electrophysiological studies
are recommended as first evaluation steps.
61. In patients with palpitations associated with
syncope, electrocardiographic monitoring and echo-
cardiography are recommended as first evaluation steps.
62. In patients with chest pain suggestive of ischaemia
before or after loss of consciousness, stress testing,
echocardiography, and electrocardiographic monitoring
are recommended as first evaluation steps.
63. In young patients without suspicion of heart or
neurological disease and recurrent syncope, tilt testing
and, in older patients, carotid sinus massage are
recommended as first evaluation steps.
64. In patients with syncope occurring during neck turn-
ing, carotid sinus massage is recommended at the outset.
65. In patients with syncope during or after effort,
Task Force Report 1263
Eur Heart J, Vol. 22, issue 15, August 2001
67. In patients with signs of autonomic failure or
neurological disease a specific diagnosis should be made.
Initial evaluation
The following section provides specific recommenda-
tions about how to use the history, physical examination
and ECG for making certain or presumptive diagnoses
of syncope.
History and physical examination
The history alone may be diagnostic of the cause of
syncope or may suggest the strategy of evaluation. The
clinical features of the presentation are most important,
especially the factors that might predispose to syncope
and its sequelae. Some attempts have been made to
validate the diagnostic value of the history in prospec-
tive and case-control studies[3,26,46–48]
.
The important parts of the history are listed in Table
2.1. They are the key features in the diagnostic work-up
of patients with syncope. When taking history, all the
items listed in the Table 2.1 should be carefully sought.
Apart from being diagnostic, the history may guide
the subsequent evaluation strategy. For example, a
cardiac cause is more likely when syncope is preceded by
palpitations or occurs in the supine position or during
exercise. Conversely, a neurally-mediated mechanism is
likely when predisposing factors, precipitating events
and accompanying symptoms are present and the
patient has recurrent syncopal episodes over several
years.
Physical findings that are useful in diagnosing syncope
include cardiovascular and neurological signs and ortho-
static hypotension. For example, the presence of a
murmur or severe dyspnoea is indicative of structural
heart disease and of a cardiac cause of syncope.
Table 2.2 lists how to use the history and physical
findings in suggesting various aetiologies.
Baseline electrocardiogram
An initial ECG is most commonly normal in patients
with syncope. When abnormal, the ECG may disclose
an arrhythmia associated with a high likelihood of
syncope, or an abnormality which may predispose to
arrhythmia development and syncope. Moreover, any
abnormality of the baseline ECG is an independent
predictor of cardiac syncope or increased mortality,
suggesting the need to pursue evaluation for cardiac
causes in these patients. Equally important, a normal
ECG is associated with a low risk of cardiac syncope as
the cause, with a few possible exceptions, for example in
cases of syncope due to a paroxysmal atrial tachy-
arrhythmia.
Arrhythmias that are considered diagnostic of the
cause of syncope are listed below. More commonly, the
baseline ECG leads to a suspected cardiac arrhythmia,
which needs to be confirmed by direct testing
(Table 2.3).
Recommendations
Diagnosis
Class I:
The results of the initial evaluation (history, physical
examination, orthostatic blood pressure measurements
Table 2.1 Important historical features
Questions about circumstances just prior to attack
69. Activity (rest, change in posture, during or after exercise, during or immediately after
urination, defaecation, cough or swallowing)
70. Predisposing factors (e.g. crowded or warm places, prolonged standing, post-prandial
period) and of precipitating events (e.g. fear, intense pain, neck movements);
Questions about onset of attack
71. Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or
shoulders, blurred vision
Questions about attack (eyewitness)
72. Way of falling (slumping or kneeling over), skin colour (pallor, cyanosis, flushing), duration
of loss of consciousness, breathing pattern (snoring), movements (tonic, clonic, tonic-clonic
or minimal myoclonus, automatism) and their duration, onset of movement in relation to
fall, tongue biting
Questions about end of attack
73. Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin colour, injury,
chest pain, palpitations, urinary or faecal incontinence
Questions about background
74. Family history of sudden death, congenital arrhythmogenic heart disease or fainting
79. (In case of recurrent syncope) Information on recurrences such as the time from the first
syncopal episode and on the number of spells
1264 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
80. and ECG) are diagnostic of the cause of syncope in the
following situations:
81. Vasovagal syncope is diagnosed if precipitating
events such as fear, severe pain, emotional distress,
instrumentation or prolonged standing are associated
with typical prodromal symptoms.
82. Situational syncope is diagnosed if syncope occurs
during or immediately after urination, defaecation,
cough or swallowing.
83. Orthostatic syncope is diagnosed when there is docu-
mentation of orthostatic hypotension associated with
syncope or pre-syncope. Orthostatic blood pressure
measurements are recommended after 5 min of lying
supine. Measurements are then continued after 1 or
3 min of standing and further continued, if blood press-
ure is still falling at 3 min. If the patient does not
tolerate standing for this period, the lowest systolic
blood pressure during the upright posture should be
recorded. A decrease in systolic blood pressure
d20 mmHg or a decrease of systolic blood pressure to
90 mmHg is defined as orthostatic hypotension
regardless of whether or not symptoms occur[49]
.
84. Cardiac ischaemia-related syncope is diagnosed
when symptoms are present with ECG evidence of
acute ischaemia with or without myocardial infarction,
independently of its mechanism*.
85. Arrhythmia-related syncope is diagnosed by ECG
when there is:
*Note. In the case of ischaemic syncope, the mechanism can be
cardiac (low output or arrhythmia) or reflex (Bezold-Jarish reflex),
but management is primarily that of ischaemia
Table 2.2 Clinical features suggestive of specific causes of real or apparent loss of
consciousness
Symptom or finding Possible cause
103. Frequent attack with somatic complaints, no
organic heart disease
Psychiatric illness
Table 2.3 ECG abnormalities suggesting an arrhythmic syncope
104. Bifascicular block (defined as either left bundle branch block or right bundle branch block
combined with left anterior or left posterior fascicular block)
110. Right bundle branch block pattern with ST-elevation in leads V1-V3 (Brugada syndrome)
111. Negative T waves in right precordial leads, epsilon waves and ventricular late potentials
suggestive of arrhythmogenic right ventricular dysplasia
112. Q waves suggesting myocardial infarction
Task Force Report 1265
Eur Heart J, Vol. 22, issue 15, August 2001
113. –Sinus bradycardia 40 beats . min 1
or repetitive
sinoatrial blocks or sinus pauses 3 s
–Mobitz II 2nd or 3rd-degree atrioventricular block
–Alternating left and right bundle branch block
–Rapid paroxysmal supraventricular tachycardia or
ventricular tachycardia
–Pacemaker malfunction with cardiac pauses
Echocardiogram
Echocardiography is frequently used as a screening test
to detect cardiac disease in patients with syncope.
Although numerous published case reports have sug-
gested an important role of echocardiography in disclos-
ing the cause and/or mechanism of syncope, larger
studies have shown that the diagnostic yield from
echocardiography is low in the absence of clinical,
physical or electrocardiographic findings suggestive of a
cardiac abnormality[50–52]
. In patients with syncope or
pre-syncope and normal physical examination, the most
frequent (from 4·6% to 18·5% of cases) finding is mitral
valve prolapse[51]
. This may be coincidental as both
conditions are common. Other cardiac abnormalities
include valvular diseases (most frequently aortic
stenosis), cardiomyopathies, regional wall motion
abnormalities suggestive of myocardial infarction,
infiltrative heart diseases such as amyloidosis, cardiac
tumours, aneurysms, atrial thromboembolism and other
abnormalities[53–66]
. Even if echocardiography alone is
only seldom diagnostic, this test provides information
about the type and severity of underlying heart disease
which may be useful for risk stratification. If moderate
to severe structural heart disease is found, evaluation is
directed toward a cardiac cause of syncope. On the other
hand, in the presence of minor structural abnormalities
detected by echocardiography, the probability of a car-
diac cause of syncope may not be high, and the evalu-
ation may proceed as in patients without structural heart
disease.
Examples of heart disease in which cardiac syncope is
likely include:
126. Echocardiography only makes a diagnosis in severe
aortic stenosis and atrial myxoma.
Carotid sinus massage
It has long been observed that pressure at the site where
common carotid artery bifurcates produces a reflex
slowing in heart rate and a fall in blood pressure. In
some patients with syncope, especially those 40 years,
an abnormal response to carotid massage can be
observed. A ventricular pause lasting 3 s or more and a
fall in systolic blood pressure of 50 mmHg or more
is considered abnormal and defines the carotid sinus
hypersensitivity[67,68]
.
The carotid sinus reflex arc is composed of an afferent
limb arising from the mechanoreceptors of the carotid
artery and terminating in midbrain centres, mainly the
vagus nucleus and the vasomotor centre. The efferent
limb is via the vagus nerve and the parasympathetic
ganglia to the sinus and atrioventricular nodes and via
the sympathetic nervous system to the heart and the
blood vessels. Whether the site of dysfunction resulting
in a hypersensitive response to the massage is central
at the level of brainstem nuclei or peripheral at the
level of carotid baroreceptors is still a matter of
debate[68–70]
.
Methodology and response to carotid sinus massage
Carotid sinus massage is a tool used to disclose carotid
sinus syndrome in patients with syncope.
Protocol. In most studies carotid sinus massage is per-
formed in the supine position; in others, it is performed
in both supine and upright positions (usually on a tilt
table). Continuous electrocardiographic monitoring
must be used. Continuous blood pressure monitoring,
for which a non-invasive measurement device is best
suited, should also be used as the vasodepressor
response is rapid and cannot be adequately detected
with devices which do not measure continuous blood
pressure. After baseline measurements, the right carotid
artery is firmly massaged for 5–10 s at the anterior
margin of the sternocleomastoid muscle at the level of
the cricoid cartilage. After 1 or 2 min a second massage
is performed on the opposite side if the massage on one
side failed to yield a ‘positive’ result. If an asystolic
response is evoked, to assess the contribution of the
vasodepressor component (which may otherwise be hid-
den) the massage is usually repeated after intravenous
administration of atropine (1 mg or 0·02 mg . kg 1
).
Atropine administration is preferred to temporary dual
chamber pacing as it is simple, non-invasive, and easily
reproducible[71]
. The response to carotid sinus massage
is generally classified as cardioinhibitory (i.e. asystole),
vasodepressive (fall in systolic blood pressure) or mixed.
1266 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
127. The mixed response is diagnosed by the association of
an asystole of d3 s and a decline in systolic blood
pressure of d50 mmHg on rhythm resumption from the
baseline value.
There are two widely used methods of carotid sinus
massage. In the first method, the massage is performed
only in the supine position and pressure is applied for no
more than 5 s. A positive response is defined as a
ventricular pause d3 s and/or a fall in systolic blood
pressure d50 mmHg. Pooled data from four studies
performed in elderly patients with syncope show a
positive rate of 35% (235 of 663 patients)[72–75]
. How-
ever, abnormal responses are also frequently observed in
subjects without syncope. For example, an abnormal
response was observed in 17%–20% of patients affected
by various types of cardiovascular diseases[32,76]
, and in
38% of patients with severe narrowing of the carotid
arteries[77]
. Moreover, the diagnosis may be missed in
about one-third of cases if only supine massage is
performed[78,79]
.
In the second method, reproduction of spontaneous
symptoms is required during carotid massage[80]
. Elicit-
ing symptoms requires a longer period of massage (10 s)
and massage performed in both supine and upright
positions[81,82]
. A positive response was observed in 49%
of 100 patients with syncope of uncertain origin[83]
and
in 60% of elderly patients with syncope and sinus
bradycardia[84]
, but only in 4% of 101 control patients
without syncope pooled from three studies[82–84]
. In an
intra-patient comparison study[82]
, the ‘method of symp-
toms’ appears to carry a higher positivity rate (49% vs
41%) in patients with syncope and a lower positivity rate
(5% vs 15%) in patients without syncope than the first
method.
Whatever method is used, increasing importance has
been given to the execution of the massage in the upright
position, usually using a tilt table[78,79,85]
. Other than a
higher positivity rate compared with supine massage
only, the importance of performing upright massage is
due to the better possibility of evaluating the magnitude
of the vasodepressor component. Under-estimated in the
past, a vasodepressor component of the reflex is present
in most patients with an asystolic response[85]
. A correct
determination of the vasodepressor component of the
reflex is of practical importance for the choice of
therapy. Indeed, pacemaker therapy has been shown to
be less effective in mixed forms with an important
vasodepressor component than in dominant cardio-
inhibitory forms[71,81]
.
Reproducibility. A concordance between abnormal and
normal responses during a second carotid sinus massage
was reported in 93% of cases[76]
. In another study[81]
, a
pause 3 s was repeatedly reproduced in all patients
who were referred for implantation of pacemaker
because of severe carotid sinus syndrome.
Complications. The main complications of carotid sinus
massage are neurological[86]
. In one study[86]
, seven
neurological complications were reported among 1600
patients (5000 massages) with an incidence of 0·45%. In
another study[87]
, 11 neurological complications were
reported in 4000 patients (16 000 massages) with an
incidence of 0·28%. These complication rates apply to
5 s of carotid sinus massage supine/upright.
Even if these complications are rare, carotid massage
should be avoided in patients with previous transient
ischaemic attacks or stroke within the past 3 months
(except when carotid Doppler studies excluded signifi-
cant stenosis) or in patients with carotid bruits[86]
.
Rarely, carotid massage may elicit self-limited atrial
fibrillation of little clinical significance[67,72]
. Since
asystole induced by the massage is self-terminating
shortly after the end of the massage, usually no
resuscitative measures are needed.
Personnel. As it carries potential hazards, the test
should be performed by physicians who are aware that
complications, especially neurological, may occur.
Relationship between carotid sinus massage and
spontaneous syncope
The relationship between carotid sinus hypersensitivity
and spontaneous, otherwise unexplained, syncope has
been demonstrated by pre-post comparative studies, two
controlled trials, and a prospective observational study
(level B). Pre-post comparisons were done by analysing
the recurrence rates of syncope in patients treated by
pacing in several non-randomized studies[88–91]
. These
studies show fewer recurrences at follow-up. One non-
randomized comparative study of patients receiving a
pacemaker and untreated patients showed syncope
recurrence rates to be lower in paced than non-paced
patients[92]
. Brignole et al.[81]
undertook a randomized
study in 60 patients; 32 patients were assigned to the
pacemaker arm and 28 to the ‘no treatment’ group.
After a mean follow-up of 36 10 months, syncope
recurred in 9% of the pacemaker group vs 57% in the
untreated patients (P0·0002). Finally, in patients
implanted with a pacemaker designed to detect asystolic
episodes, long pauses (d6 s) were detected in 53% of the
patients during 2 years of follow-up, suggesting that a
positive response to carotid massage predicts the occur-
rence of spontaneous asystolic episodes[93]
.
Recommendations
Indications and methodology
Class I:
128. Carotid sinus massage is recommended in patients
over age 40 years with syncope of unknown aetiology
after the initial evaluation. In case of risk of stroke
due to carotid artery disease, massage should be
avoided.
129. Electrocardiographic monitoring and continuous
blood pressure measurements during carotid massage is
mandatory. Duration of massage of a minimum of 5 and
a maximum of 10 s is recommended. Carotid massage
should be performed with the patient both supine and
erect.
Task Force Report 1267
Eur Heart J, Vol. 22, issue 15, August 2001
131. The procedure is considered positive if symptoms are
reproduced during or immediately after the massage in
the presence of asystole longer than 3 s and/or a fall in
systolic blood pressure of 50 mmHg or more. A positive
response is diagnostic of the cause of syncope in the
absence of any other competing diagnosis.
Tilt testing
Background
On moving from supine to erect posture there is a large
gravitational shift of blood away from the chest to the
distensible venous capacitance system below the dia-
phragm. This shift is estimated to total one half to one
litre of thoracic blood and the bulk of the total change
occurs in the first 10 s. In addition, with prolonged
standing, the high capillary transmural pressure in
dependent parts of the body causes a filtration of
protein-free fluid into the interstitial spaces. It is esti-
mated that this results in about a 15–20% (700 ml)
decrease in plasma volume in 10 min in healthy hu-
mans[9]
. As a consequence of this gravitationally induced
blood pooling and the superimposed decline in plasma
volume, the return of venous blood to the heart is
reduced resulting in a rapid diminution of cardiac filling
pressure and thereby in a decrease in stroke volume.
Despite decreased cardiac output, a fall in mean arterial
pressure is prevented by a compensatory vasoconstric-
tion of the resistance and the capacitance vessels in the
splanchnic, musculo-cutaneous, and renal vascular beds.
Vasoconstriction of systemic blood vessels is the key
factor in the maintenance of arterial blood pressure in
the upright posture. Pronounced heart rate increases are
insufficient to maintain cardiac output: the heart cannot
pump blood that it does not receive[9]
. The rapid short-
term adjustments to orthostatic stress are mediated
exclusively by the neural pathways of the autonomic
nervous system. During prolonged orthostatic stress,
additional adjustments are mediated by the humoral
limb of the neuroendocrine system[9]
. The main sensory
receptors involved in orthostatic neural reflex adjust-
ments are the arterial mechanoreceptors (baroreceptors)
located in the aortic arch and carotid sinuses.
Mechanoreceptors located in the heart and the lungs
(cardiopulmonary receptors) are thought to play a
minor role. Reflex activation of central sympathetic
outflow to the systemic blood vessels can be reinforced
by local reflex mechanisms like the venoarteriolar reflex.
The skeletal muscle pump and the respiratory pump
play an important adjunctive role in the maintenance of
arterial pressure in the upright posture by promoting
venous return. The static increase in skeletal muscle tone
induced by the upright posture opposes pooling of blood
in limb veins even in the absence of movement of the
subject[9]
. Failure of such compensatory adjustments to
orthostatic stress is thought to play a predominant role
in a large number of patients with syncope. This forms
the basis for the use of tilt testing in the evaluation of
patients with syncope. There is a large body of literature
on the mechanisms involved in vasovagal syncope
induced by tilt testing. Yet many unanswered questions
remain regarding the multiple potential causes and the
underlying pathophysiology. The panel did not consider
an extensive review of pathophysiology as one of the
goals of the consensus process. Excellent reviews are
available[94–97]
.
Tilt test protocols
In 1986 Kenny et al.[98]
observed an abnormal response
to tilt test in 10 out of 15 patients with syncope of
unknown origin. This response consisted of hypotension
and/or bradycardia. They also performed the test in 10
healthy controls without previous syncope, and an
abnormal response was provoked in only one. In this
study, the authors used an inclination of 60 during
60 min of tilt duration. Since then, tilt testing has been
used extensively by many authors proposing different
protocols for diagnostic, investigational and therapeutic
purposes. Tilt testing protocols have varied with respect
to many factors including the angle of tilting, time
duration and the use of different provocative drugs.
In 1991, Fitzpatrick et al.[99]
showed that the use of a
bicycle saddle with the legs hanging free for tilt testing
gave a low specificity when compared with footboard
support. They also showed that tilting at an angle of less
than 60 resulted in a low rate of positive responses.
Analysing the time to positive responses, they reported a
mean time of 24 10 min and proposed 45 min of
passive tilting as an adequate duration for the test since
this incorporated the mean duration to syncope plus two
standard deviations. This method is widely known as the
Westminster protocol. They reported a rate of positive
responses in patients with syncope of unknown origin of
75% and a specificity of 93%.
In 1989, Almquist et al.[100]
and Waxman et al.[101]
used intravenous isoproterenol during tilt testing. In the
study of Almquist et al.[100]
, after 10 min of passive tilt
test without drugs, patients were returned to the supine
position and an isoproterenol infusion at initial doses of
1 g . min 1
was administered. When patients achieved
a stable increase in heart rate they were tilted again. This
manoeuvre was repeated at increasing doses up to
5 g . min 1
. With this protocol nine of 11 patients with
syncope of unknown origin and negative electrophysio-
logical study showed hypotension and/or bradycardia,
whereas such responses were found in only two of
18 control subjects. In 1992, Kapoor et al.[102]
using
an isoproterenol tilt test at 80 , in which isoproterenol
was administered in progressive doses from 1 to
5 g . min 1
, without returning the patient to the supine
position before each dose increase, reported a low
specificity (between 45% and 65%). In 1995, Morillo
et al.[103]
and Natale et al.[104]
proposed a ‘shortened’
low-dose isoproterenol tilt test, in which, after 15–
20 min of baseline tilt at 60–70 , incremental doses of
isoproterenol designed to increase average heart rate by
about 20–25% over baseline (usually c3 g . min 1
)
1268 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
132. were administered without returning the patient to the
supine position in one study, or returning to the supine
position in the other. With this protocol, the rate of
positive responses was of 61% with a specificity of
92–93%.
In 1994, Raviele et al.[105]
proposed the use of intra-
venous nitroglycerin infusion. With their protocol, 21 of
40 (53%) patients with syncope of unknown origin had
positive responses with a specificity of 92%. Ten of 40
patients (25%), had progressive hypotension without
bradycardia. This response was classified as an exagger-
ated response consisting of an excessive hypotensive
effect of the drug. More recently Raviele et al.[106]
have
used sublingual nitroglycerin instead of an intravenous
infusion. After 45 min of baseline tilting, 0·3 mg of
sublingual nitroglycerin was administered. With this
protocol, the overall rate of positive responses in
patients with syncope of unknown origin was 51% (25%
with baseline tilt test and 26% after nitroglycerin admin-
istration) with a specificity of 94%. An exaggerated
response was observed in 14% of patients and 15% of
controls. The main advantage of sublingual nitro-
glycerin is that venous cannulation is not needed for the
protocol. Oraii et al.[107]
and Raviele et al.[108]
have
compared the isoproterenol test with the nitroglycerin
test, with similar rates of positive responses and specifi-
city, but with a lower rate of side effects with nitro-
glycerin. The optimal duration of the unmedicated phase
before the administration of sublingual nitroglycerin has
not been fully established. Bartoletti et al.[109]
compared
the effect of an unmedicated phase of 45 min vs 5 min on
the overall positive rate of the nitroglycerin test. The test
with the short passive phase was associated with a
significant reduction in the rate of positive responses,
and they concluded that at least some baseline unmedi-
cated tilt testing is needed. Recently, many authors
have used a shortened protocol using 400 g nitro-
glycerin spray sublingually after a 20 min baseline
phase. Pooled data from three studies[110–112]
using this
protocol, in a total of 304 patients, showed a positive
response rate of 69% which was similar to the positive
rate of 62% observed in 163 patients from three other
studies[109,112,113]
using a passive phase duration of
45 min and 400 g nitroglycerin spray administration.
With this protocol, specificity remained high, being
94% in 97 controls[110–112]
. Thus a 20 min passive phase
before nitroglycerin administration appears to be an
alternative to the more prolonged 45 min passive phase.
This method is known as the Italian protocol.
Other drugs used as provocative agents during
tilt testing include isosorbide dinitrate[114,115]
, edro-
phonium[116,117]
, clomipramine[118]
and adenosine; the
latter is discussed in another section.
Irrespective of the exact protocol, some general
measures may be suggested when tilt testing is per-
formed. Many of the following rules were published in
1996 as an expert consensus document[119]
. The room
where the test is performed should be quiet and with dim
lights. The patients should fast for at least 2 h before
the test. The patients should be in a supine position
20–45 min before tilting. This time interval was pro-
posed to decrease the likelihood of a vasovagal reaction
in response to venous cannulation[120,121]
. With the
protocols that do not use venous cannulation, time in
the supine position before tilting can be reduced to
5 min. Continuous beat-to-beat finger arterial blood
pressure should be monitored non-invasively[122]
.
Invasive measurements of arterial blood pressure
can affect the specificity of the test, especially in the
elderly[120]
and in children[121]
. Although intermittent
measurement of pressure using a sphygmomanometer is
less desirable, it is an accepted method of testing and is
widely used in clinical practice, especially in children.
The tilt table should be able to achieve the upright
position smoothly and rapidly and to reset to the supine
position quickly (10 s) when the test is completed in
order to avoid the consequences of prolonged loss of
consciousness. Only tilt tables with foot-board support
are appropriate for syncope evaluation. An experienced
nurse or medical technician should be in attendance
during the entire procedure. The need for a physician to
be present throughout the tilt test procedure is less well
established because the risk to patients of such testing is
very low. Therefore, it is sufficient that a physician is in
proximity and immediately available should a problem
arise.
Recommended tilt test protocols
Class I:
133. Supine pre-tilt phase of at least 5 min when no
venous cannulation is performed, and at least 20 min
when cannulation is undertaken.
136. Use of ether intravenous isoproterenol/isoprenaline
or sublingual nitroglycerin for drug provocation if
passive phase has been negative. Drug challenge phase
duration of 15–20 min.
137. For isoproterenol, an incremental infusion rate from
1 up to 3 g . min 1
in order to increase average heart
rate by about 20–25% over baseline, administered
without returning the patient to the supine position.
138. For nitroglycerin, a fixed dose of 400 g nitro-
glycerin spray sublingually administered in the upright
position.
139. The end-point of the test is defined as induction of
syncope or completion of the planned duration of tilt
including drug provocation. The test is considered
positive if syncope occurs.
Class II:
Divergence of opinion exists in the case of induction of
pre-syncope.
Responses to the tilt test
In 1992, Sutton et al.[123]
, using the details of haemo-
dynamic responses to tilt testing, proposed a classifica-
tion of the positive responses, which has been recently
modified[124]
. This classification is shown in the
Table 2.4.
Task Force Report 1269
Eur Heart J, Vol. 22, issue 15, August 2001
140. Since the decision to terminate tilting influences the
type of response[125]
, for a correct classification of
responses tilting should be interrupted at the precise
occurrence of loss of consciousness with simultaneous
loss of postural tone[124]
. Premature interruption under-
estimates and delayed interruption over-estimates the
cardioinhibitory response and exposes the patient to the
consequences of prolonged loss of consciousness. How-
ever, a consensus does not exist in this regard and many
physicians consider a steadily falling blood pressure
accompanied by symptoms sufficient to stop the test.
Some authors[105,106,124,126]
have analysed the be-
haviour of blood pressure and heart rate during the
period of upright position which precedes the onset of
the vasovagal reaction. Different patterns have been
recognized. To summarize, two of these are the most
frequent. The typical pattern is characterized by an
initial phase of rapid and full compensatory reflex
adaptation to the upright position resulting in a
stabilization of blood pressure and heart rate (which
suggests normal baroreflex function) to the time of an
abrupt onset of the vasovagal reaction. The patients
with this pattern are largely young and healthy; they
have a long history of several syncopal episodes; in
many cases the first syncopal episodes occurred in the
teenage years; secondary trauma is infrequent. This
pattern, also called ‘Classic’, is felt to represent a ‘hyper-
sensitive’ autonomic system that over-responds to vari-
ous stimuli. Conversely, a different pattern is frequently
observed that is characterized by an inability to obtain a
steady-state adaptation to the upright position and,
therefore, a progressive fall in blood pressure and heart
rate occurs until the onset of symptoms. The cause of
symptoms in this case seems to be an inability to adapt
promptly to some external influences (‘hyposensitive’
autonomic function). Different subtypes have been
described with slight differences between them. The
patients affected are mostly old and many have associ-
ated diseases; they have a short history of syncope with
few episodes per patient; syncopal episodes begin late in
life, suggesting they are due to the occurrence of some
underlying dysfunction. This pattern resembles that seen
in patients with autonomic failure and suggests that an
overlap between typical vasovagal syncope and more
complex disturbances of the autonomic nervous system
exists. Tilt testing can be useful to discriminate between
these two syndromes.
Role of head-up tilt test in treatment selection for
vasovagal syncope
In order to use tilt testing effectively in the evaluation of
the therapeutic options, two conditions are needed: a
high reproducibility of the test and responses to tilt
testing that are predictive of outcomes at follow-up.
The reproducibility of tilt testing has been widely
studied[127–131]
. The overall reproducibility of an initial
negative response (85% to 94%) is higher than the
reproducibility of an initial positive response (31% to
92%). In addition, data from controlled trials showed
that approximately 50% of patients with a baseline
positive tilt test became negative when the test was
repeated with treatment or with placebo[132–134]
. More-
over, acute studies were not predictive of the long-term
outcome of pacing therapy[135]
. These data show that the
use of tilt testing for assessing the effectiveness of
different treatments has important limitations (level A).
Complications
Head-up tilt test is a safe procedure and the rate of
complications is very low. Although asystolic pauses as
long as 73 s have been reported[136]
the presence of such
prolonged asystole during a positive response cannot be
considered a complication, since this is an end-point of
the test. A rapid return to the supine position as soon as
syncope occurs is usually all that is needed to prevent or
to limit the consequences of prolonged loss of conscious-
ness; brief resuscitation manoeuvres are seldom needed.
Case reports have documented life-threatening ventricu-
lar arrhythmias with isoproterenol in the presence of
ischaemic heart disease[137]
or sick sinus syndrome[138]
.
No complications have been published with the use of
nitroglycerin. Minor side effects are common and in-
clude palpitations with isoproterenol and headache with
nitroglycerin. Atrial fibrillation can be induced during or
after a positive tilt test and is usually self-limited[139]
.
Table 2.4 Classification of positive responses to tilt testing
141. Type 1 Mixed. Heart rate falls at the time of syncope but the ventricular rate does not fall
to less than 40 beats . min 1
or falls to less than 40 beats . min 1
for less than 10 s with or
without asystole of less than 3 s. Blood pressure falls before the heart rate falls.
142. Type 2A Cardioinhibition without asystole. Heart rate falls to a ventricular rate less than
40 beats . min 1
for more than 10 s but asystole of more than 3 s does not occur. Blood
pressure falls before the heart rate falls.
143. Type 2B Cardioinhibition with asystole. Asystole occurs for more than 3 s. Blood pressure
fall coincides with or occurs before the heart rate fall.
144. Type 3 Vasodepressor. Heart rate does not fall more than 10% from its peak at the time of
syncope.
145. Exception 1. Chronotropic Incompetence. No heart rate rise during the tilt testing (i.e. less
than 10% from the pre-tilt rate).
146. Exception 2. Excessive heart rate rise. An excessive heart rate rise both at the onset of the
upright position and throughout its duration before syncope (i.e. greater than
130 beats . min 1
).
1270 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
148. In cases of unexplained single syncopal episodes in
high risk settings (e.g. occurrence of, or potential risk
for, physical injury or with occupational implications),
or recurrent episodes in the absence of organic heart
disease, or, in the presence of organic heart disease,
after cardiac causes of syncope have been excluded.
149. When it will be of clinical value to demonstrate
susceptibility to neurally-mediated syncope to the
patient.
Class II:
Tilt testing is indicated for diagnostic purposes:
150. When an understanding of the haemodynamic
pattern in syncope may alter the therapeutic approach.
155. A single episode without injury and not in a high risk
setting.
156. Clear-cut clinical vasovagal features leading to a
diagnosis when demonstration of a neurally mediated
susceptibility would not alter treatment.
Diagnosis
Class I:
157. In patients without structural heart disease, tilt
testing can be considered diagnostic, and no further
tests need to be performed when spontaneous syncope is
reproduced.
158. In patients with structural heart disease, arrhythmias
or other cardiac causes should be excluded prior
to considering positive tilt test results as evidence
suggesting neurally mediated syncope.
Class II:
159. The clinical meaning of abnormal responses other
than induction of syncope is unclear.
Electrocardiographic monitoring
(non-invasive and invasive)
ECG monitoring is a procedure for diagnosing intermit-
tent brady- and tachyarrhythmias. However, the tech-
nology of ECG monitoring currently has serious
limitations.
Indications
Patients with very infrequent syncope, recurring over
months or years, are unlikely to be diagnosed by con-
ventional Holter monitoring, since the likelihood of
symptom–ECG correlation is very low. Consideration
should be given to conventional event recording in such
patients, but this technique has important logistical
limitations that might prevent a successful ECG record-
ing during syncope. Patients with syncope often have
significant arrhythmia, infrequent recurrences, and
sudden loss of consciousness and recover quickly.
In such circumstances where the interval between recur-
rences is measured in months or years, consideration
should be given to implantable ECG loop recorder.
Holter monitoring in syncope.
Most ECG monitoring in syncope is undertaken with
external 24 h cassette tape-recorders connected to the
patient via external wiring and adhesive ECG patches.
Advantages include: it is a non-invasive test; there
is beat-to-beat acquisition; device costs are low and
there is relatively high fidelity over short time-periods.
Limitations include: patients may not tolerate adhesive
electrodes or electrodes may not remain adherent
throughout monitoring or during an event.
A recurrence of presenting symptoms may not occur
during monitoring. The vast majority of patients have a
syncope-free interval measured in weeks, months or
years, but not days and, therefore, symptom–ECG cor-
relation can rarely be achieved with Holter monitoring.
In an overview[140]
of the results of eight studies of
ambulatory monitoring in syncope, only 4% of patients
(range between 6 and 20%) had correlation of symptoms
with arrhythmia. The true yield of conventional ECG
monitoring in syncope may be as low as 1–2% in an
unselected population[141–143]
. Admittedly, in 15% of
patients, symptoms were not associated with arrhyth-
mia. Thus in these patients, a rhythm disturbance could
potentially be excluded as a cause of syncope.
An asymptomatic arrhythmia detected by Holter
monitoring is often used to make a diagnosis by infer-
ence, but, without symptom–ECG correlation, there is
potential for ECG findings to be inappropriately maxi-
mized leading to unnecessary therapy, e.g. pacemaker
implantation in a patient with vasomotor syncope.
Alternatively, there is potential for symptoms to be
inappropriately minimized by physicians if Holter
monitoring fails to yield any evidence of an arrhythmia.
Holter monitoring in syncope is therefore cheap in
terms of set-up costs, but expensive in terms of cost-per-
diagnosis; whilst unnecessary analysis of asymptomatic
tapes might be avoidable by analysis only of sympto-
matic tapes. Such a strategy would require further
provision of very large numbers of tape-recorders,
greatly increasing the cost. Holter monitoring in
syncope may be of more value if symptoms are very
frequent. Daily single or multiple episodes of loss-of-
consciousness might increase the potential for
symptom–ECG correlation. However, experience in
these patients suggests that many have psychogenic
blackouts. Undoubtedly, in such patients, true nega-
tive findings of Holter monitoring may be useful in
confirming the underlying cause.
External ECG event monitoring in syncope
Conventional event recorders are external devices
equipped with fixed electrodes through which an ECG
Task Force Report 1271
Eur Heart J, Vol. 22, issue 15, August 2001
160. can be recorded by direct application to the chest wall.
Provided the patient can comply at the time of symp-
toms, a high-fidelity recording can be made. Recordings
can be prospective or retrospective (loop recorders) or
both. Some recorders have long-term cutaneous patch
connections, making a good skin contact for recordings
less crucial. Prospective external event recorders have a
limited value in syncope because the patient must be able
to apply the recorder to the chest during the period of
unconsciousness and activate recording. In one
study[144]
, external retrospective loop recorders showed
relatively higher diagnostic yield in syncope, 25% of
enrolled patients having syncope or pre-syncope
recorded during the monitoring period up to 1 month,
but comparisons with Holter monitoring are not
possible because the study used highly selected patients
with relatively high recurrence of syncope. However,
since patients usually do not comply for more than a few
weeks with this instrument, symptom–ECG correlation
cannot be achieved when the syncopal recurrence rate is
less frequent.
Implantable ECG event monitoring in syncope
Recently an implantable ECG event monitor
(Implantable Loop Recorder) has become available.
This device is placed subcutaneously under local
anaesthesia, and has a battery life of 18–24 months.
High fidelity ECG recordings can be made. The
device has a solid-state loop memory, and the current
version can store up to 42 min of continuous ECG.
Retrospective ECG allows activation of the device after
consciousness has been restored. In a small series of
highly selected patients, symptom–ECG correlation was
achieved in 88% of patients within a mean of 5 months
of implantation[145]
. In a larger series[146]
, symptom–
ECG correlation was achieved in 59% of 85 patients
within a mean of 10 months of implantation. Syncope–
ECG correlation was achieved in 27% of patients and
pre-syncope–ECG correlation in 32%; pre-syncope was
much less likely to be associated with an arrhythmia
than syncope and did not prove to be an accurate
surrogate for syncope in establishing a diagnosis
(level B).
Advantages of the Implantable Loop Recorder
include: continuous loop high-fidelity ECG recording
for up to 24 months; a loop memory which allows
activation after consciousness is restored; removal of
logistical factors which prevent good ECG recording
during symptoms; and a potential for a high yield in
terms of symptom–ECG correlation because of the high
likelihood of recording during recurrence of presenting
symptoms.
Disadvantages include: the need for a minor surgical
procedure; the lack of recording of any other concurrent
physiological parameter, e.g. blood pressure; the current
need for patient activation, though data suggest that this
is usually possible after recovery of consciousness (now
avoided by automatic versions); the high cost of the
implantable device.
The implantable loop recorder carries a high up-front
cost. However, if symptom–ECG correlation can be
achieved in a substantial number of patients within 12
months of implantation, then analysis of the cost per
symptom–ECG yield could show that the implanted
device may be more cost-effective that a strategy using
conventional investigation. This remains to be
confirmed[145–147]
.
From the initial experience in patients with unex-
plained syncope, it appears that the Implantable Loop
Recorder might become the reference standard to be
adopted when an arrhythmic cause of syncope is sus-
pected but not sufficiently proven to allow an aetiologi-
cal treatment. There are several areas of interest:
patients who have a diagnosis of neurally-mediated
syncope when the understanding of the exact mechanism
of spontaneous syncope may alter the therapeutic
approach; patients with bundle branch block in whom a
paroxysmal AV block is likely despite a complete nega-
tive electrophysiological evaluation; patients with severe
left ventricular dysfunction and non-sustained ventricu-
lar tachyarrhythmias in whom a ventricular tachy-
arrhythmia is likely despite a completed negative
electrophysiological study.
ECG monitoring in syncope — where in the work-up?
The role of ECG monitoring in syncope cannot be
defined in isolation. Physicians may be guided by the
results of clinical history, physical examination and
objective testing, for example, by tilt testing. Under
some situations where the clinical evidence strongly
suggests a diagnosis of reflex syncope, ECG monitoring
may be deemed unnecessary. This is especially the case if
symptoms are infrequent. Under these circumstances,
Holter monitoring is particularly unlikely to yield a
diagnosis, and there implantable monitoring is now
considered. However, future technology may allow
recording of multiple signals in addition to the ECG and
will place emphasis on the features of spontaneous
episodes as they correlate with cardiac rhythm, rather
than provoked syncope. Knowledge of what transpires
during a spontaneous syncopal episode is the gold
standard for syncope evaluation. For this reason it
is likely that implantable monitors will become
increasingly important in syncope. Although the docu-
mentation of a bradyarrhythmia concurrent with a
syncopal episode is considered diagnostic, nevertheless
sometimes further evaluation may be necessary in order
to discriminate between an intrinsic cardiogenic
abnormality and a neurogenic mechanism; this latter
seems to be the most frequent cause of paroxysmal
bradyarrhythmias[148]
.
Recommendations
Indications
Class I:
161. Holter monitoring is indicated in patients with struc-
tural heart disease and frequent (or even infrequent)
symptoms when there is a high pre-test probability of
identifying an arrhythmia responsible for syncope.
1272 Task Force Report
Eur Heart J, Vol. 22, issue 15, August 2001
162.
163. When the mechanism of syncope remains unclear
after full evaluation, External or Implantable Loop
Recorders are recommended when there is a high
pre-test probability of identifying an arrhythmia
responsible for syncope.
Diagnosis
Class I:
164. ECG monitoring is diagnostic when a correlation
between syncope and an electrocardiographic
abnormality (brady- or tachyarrhythmia) is detected.
165. ECG monitoring excludes an arrhythmic cause when
there is a correlation between syncope and sinus
rhythm.
166. In the absence of such correlations additional testing
is recommended with the possible exception of:
–ventricular pauses longer than 3 s when awake
–periods of Mobitz II or third-degree atrioventricu-
lar block when awake
–rapid paroxysmal ventricular tachycardia
Electrophysiological testing
Transoesophageal electrophysiological study
The role of the non-invasive or transoesophageal
electrophysiological examination is limited to screening
for fast supraventricular tachycardia due to atrio-
ventricular nodal reentrant tachycardia or atrioventricu-
lar reentrant tachycardia in patients with a normal
resting ECG and a history of syncope associated with
palpitations and to the evaluation of sinus node dysfunc-
tion in patients with syncope suspected to be due to
bradycardia. It can also be used for risk evaluation in
patients with pre-excitation, although a normal refrac-
tory period of the accessory pathway cannot rule out
a risk of atrial fibrillation with a fast ventricular
response[149,150]
.
Invasive electrophysiological study
The diagnostic efficiency of the invasive electrophysio-
logical study is — like all test procedures — highly
dependent on the degree of suspicion of the abnormality
(pre-test probability), but also on the applied protocol,
and the criteria used for diagnosing the presence of
clinically significant abnormalities.
The diagnostic yield. Electrophysiological studies use
endocardial and (in the coronary sinus) epicardial
electrical stimulation and recording to disclose abnor-
malities that suggest a primary arrhythmia as the cause
of syncope. However, only a few studies have used
Holter monitoring or implantable devices to confirm the
results of the electrophysiological study. The true diag-
nostic yield of the electrophysiological study is therefore
only partly known.
Four studies[148,151–153]
have compared the findings
of the electrophysiological study with the arrhythmia
documented during a spontaneous syncopal episode by
electrocardiographic monitoring. In the study by
Fujimura et al.[151]
, the utility of the electrophysiological
study was questioned because its result suggested the
correct diagnosis only in 15% of patients, who had
syncope due to transient bradycardia. However, in that
study pharmacological provocation was not used. A
very conservative criterion for significant sinus node
dysfunction (SNRT 3000 ms) was used, and brady-
cardiac syncope due to an abnormal vagal reflex was not
excluded. Indeed, when neurally-mediated syncope was
excluded, Brignole et al.[148]
showed that the presence of
an abnormal sinus node or His-Purkinje function (at
baseline or after ajmaline provocation) disclosed the
correct diagnosis in 86% of cases with spontaneous
syncope due to sinus arrest or paroxysmal AV block,
respectively. The results of the latter study have been
corroborated in subsequent reports on patients with
either electrocardiographic monitoring performed
before electrophysiological study or by a bradycardia
detecting pacemaker after an electrophysiological
study[154,155]
. Importantly, unrelated ventricular tachy-
cardia and fibrillation and atrial tachyarrhythmias were
induced in 24% and in 20% of patients in the Fujimura
and Brignole studies, tachycardias that mistakenly might
have been designated as the cause of syncope. In patients
with syncope due to atrial or ventricular tachyarrhyth-
mias, Lacroix et al.[152]
showed that, while an electro-
physiological study reproduced the spontaneous
arrhythmia in 13 of 17 cases, a non-specific atrial or
ventricular arrhythmia was also induced in 31 of 44
cases. Finally, Moasez et al.[153]
showed that sustained
monomorphic ventricular tachycardia on Holter moni-
toring was a strong predictor of induction of the same
arrhythmia by electrophysiological study in syncopal
patients, in concordance with many other studies on
monomorphic ventricular tachycardia in patients with
ischaemic heart disease (see below).
Predictors of positive results. In an overview of eight
studies including 625 patients with syncope undergoing
electrophysiological study Linzer et al.[156]
assessed the
association between organic heart disease and an abnor-
mal test result. Ventricular tachycardia was induced in
21%, and abnormal indices of bradycardia were found in
34% of patients with organic heart disease or an abnor-
mal standard ECG. The corresponding figures were 1
and 10%, respectively, in patients with an apparently
normal heart (P0·001 for both comparisons). Thus,
positive results at electrophysiological study occur pre-
dominantly in patients with evidence of organic heart
disease (level B).
Suspected bradycardia. The pre-test probability of a
transient symptomatic bradycardia is relatively high
when there is an asymptomatic sinus bradycardia
(50 beats . min 1
) or sinoatrial block and syncope
occurs suddenly, without premonitory symptoms, is
independent of posture and physical activity, is short-
lasting, and is followed by rapid recovery. Sinus node
disease/sick sinus syndrome is present when symptoms
and sinus bradycardia or pauses occur simultaneously as
proven by ECG monitoring (‘gold standard’). Sinus
Task Force Report 1273
Eur Heart J, Vol. 22, issue 15, August 2001